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目的 研究 MDM2癌基因与野生型 p5 3基因在细胞凋亡发生中的相互关系。方法 构建了一个表达人野生型 ( wt) p5 3逆转录病毒载体 ,经 PA31 7细胞包装后转染人胰腺癌细胞 ( PC- 2 ) ,建成 PC- 2 /swtp5 3转化细胞系。再用含 MDM2基因的p CMV- MDM2载体转染 PC- 2 /swtp5 3细胞 ,获得双重转染细胞系 PC- 2 /swtp5 3/p CMV- MDM2。用流式细胞技术 ,原位检测分析和 DNA凝胶电泳分析细胞凋亡。结果 恢复 wtp5 3表达的胰腺癌细胞系 ( PC- 2 /swtp5 3)细胞凋亡明显增多 ( >1 2 % ) ,而双重转染的细胞系 ( PC- 2 /swtp5 3/p CMV- MDM2 )则凋亡细胞数明显下降 ( 3.2 % )。结论 MDM2癌基因可抑制由野生型 p5 3基因诱发的细胞凋亡。
Objective To investigate the relationship between MDM2 oncogene and wild-type p53 gene in the occurrence of apoptosis. METHODS: A human wild-type (wt) p53 retrovirus vector was constructed and transfected into human pancreatic cancer cells (PC-2) after PA31-7 cell packaging. The PC-2/swtp5 3 transformed cell line was established. The PC-2/swtp53 cells were transfected with the pCMV-MDM2 vector containing the MDM2 gene to obtain the double transfected cell line PC-2/swtp5 3/p CMV-MMM2. Flow cytometry, in situ detection analysis and DNA gel electrophoresis were used to analyze apoptosis. Results The apoptosis of the pancreatic cancer cell line (PC-2/swtp5 3) restored wtp5 3 expression was significantly increased (>1 2%), while the double transfected cell line (PC-2/swtp5 3/p CMV-MDM2). The number of apoptotic cells decreased significantly (3.2%). Conclusion MDM2 oncogene can inhibit apoptosis induced by wild-type p53 gene.